ArticleClinical cancer research : an official journal of the American Association for Cancer Research2015
The Hippo Coactivator YAP1 Mediates EGFR Overexpression and Confers Chemoresistance in Esophageal Cancer.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
163 citing papers in PubMed, 1 synthesis or guideline pooled it, 268 citations in OpenAlex.
- A Number of the N-terminal RASSF Family: RASSF7.Anti-cancer agents in medicinal chemistry · 2024Pooled it
- Trial
- Epigenetic silencing of TBX1 inactivates the Hippo pathway to potentiate chemoresistance in esophageal squamous cell carcinoma.Cell death & disease · 2026Article
- Implantation awakens peri-implant osteogenic potential via Snx5-EGFR axis-mediated mechanical transduction.International journal of oral science · 2026Article
- Degradation of the TEAD•YAP/TAZ Transcription Factor Complex by Heterobifunctional Small Molecules that Bind to the TEAD Allosteric Lipid Pocket.bioRxiv : the preprint server for biology · 2026Article
- YAP1 depletion enhances TAZ and its complexation with TEAD4 and AP-1 heterodimer C-JUN/FOSB in gastric cancer progression and metastasis.Cancer heterogeneity and plasticity · 2026Article
- Hippo-YAP/TAZ signaling in gastric cancer: orchestrating epithelial-stromal heterogeneity, plasticity, and therapy resistance.Cancer heterogeneity and plasticity · 2026Article
- Reprogrammed Fibrotic Niche Fuels Lung Cancer Initiation and Reciprocal Remodeling.International journal of biological sciences · 2026Review
- Experimental assessment of computationally nominated small molecules targeting the YAP-TEAD interface in Hippo pathway-altered mesothelioma cell models.Frontiers in oncology · 2026Article
- Activation of the Hippo Pathway by ATN Suppresses Cancer Stem-Like Properties and EGFR-Associated Signaling in Castration-Resistant Prostate Cancer CellsInternational journal of medical sciences · 2026Article
- Multidimensional Regulatory Network ofOncology research · 2026Review
- YAP as a therapeutic target in esophageal squamous cell carcinoma: insights and strategies.Annals of medicine · 2025Review
- HDAC Inhibitors Enhance the Chemosensitivity of Osteosarcoma Cells to Etoposide by Suppressing the Hippo/YAP Signaling Pathway.International journal of molecular sciences · 2025Article
- MED12 mutation induces RTK inhibitor resistance in NSCLC via MEK/ERK pathway activation by inflammatory cytokines.Cellular and molecular life sciences : CMLS · 2025Article
- TFAP2A facilitates the metastasis and radioresistance of esophageal cancer by promoting EGFR transcription.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- AT101 Suppresses Gastrointestinal Stromal Tumor Growth and Promotes Apoptosis via YAP/TAZ-CCND1 and FBXW7-MCL1 Axes.Annals of surgical oncology · 2025Article
- TET2 orchestrates YAP signaling to potentiate targetable vulnerability in hepatocellular carcinoma.Cell death & disease · 2025Article
- CDK4/6-mediated phosphorylation of DUB3 promotes YAP1 stability and hepatocellular carcinoma progression.Cell death discovery · 2025Article
- Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.Journal of hematology & oncology · 2025Review
- YAP acts as an independent prognostic marker and regulates growth and metastasis of gastrointestinal stromal tumors via FBXW7-YAP pathway.Journal of gastroenterology · 2025Article
103 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeEsophageal cancer is an aggressive malignancy and often resistant to therapy. Overexpression of EGFR has been associated with poor prognosis of patients with esophageal cancer. However, clinical trials using EGFR inhibitors have not provided benefit for patients with esophageal cancer. Failure of EGFR inhibition may be due to crosstalk with other oncogenic pathways. EXPERIMENTAL
designIn this study, expression of YAP1 and EGFR were examined in EAC-resistant tumor tissues versus sensitive tissues by IHC. Western blot analysis, immunofluorescence, real-time PCR, promoter analysis, site-directed mutagenesis, and in vitro and in vivo functional assays were performed to elucidate the YAP1-mediated EGFR expression and transcription and the relationship with chemoresistance in esophageal cancer.
resultsWe demonstrate that Hippo pathway coactivator YAP1 can induce EGFR expression and transcription in multiple cell systems. Both YAP1 and EGFR are overexpressed in resistant esophageal cancer tissues compared with sensitive esophageal cancer tissues. Furthermore, we found that YAP1 increases EGFR expression at the level of transcription requiring an intact TEAD-binding site in the EGFR promoter. Most importantly, exogenous induction of YAP1 induces resistance to 5-fluorouracil and docetaxcel, whereas knockdown of YAP1 sensitizes esophageal cancer cells to these cytotoxics. Verteporfin, a YAP1 inhibitor, effectively inhibits both YAP1 and EGFR expression and sensitizes cells to cytotoxics.
conclusionsOur data provide evidence that YAP1 upregulation of EGFR plays an important role in conferring therapy resistance in esophageal cancer cells. Targeting YAP1-EGFR axis may be more efficacious than targeting EGFR alone in esophageal cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.